Aquaporins (AQPs) have been found to be associated with a number of diseases. However, the role of AQP-1 in the pathogenesis of osteoarthritis remains unclear. We previously found that AQP-1 expression was upregulated in osteoarthritic cartilage and strongly correlated with caspase-3 expression and activity. The aim of this study was to further investigate the association of AQP-1 expression with chondrocyte apoptosis in a rat model of osteoarthritis, using RNA interference to knock down AQP-1. For this purspose, 72 male Sprague-Dawley rats were randomly assigned to 3 groups as follows: the control group not treated surgically (n=24), the sham-operated group (n=24), and the osteoarthritis group (n=24). Osteoarthritis was induced by amputating the anterior cruciate ligament and medial collateral ligament and partially excising the medial meniscus. Chondrocytes from the rats with osteoarthritis were isolated and cultured. shRNAs were used to knock down AQP-1 expression in the cultured chondrocytes. The expression of AQP-1 and caspase-3 was determined by reverse transcription-quantitative polymerase chain reaction. Caspase-3 activity was measured using a caspase-3 colorimetric assay. The rats in our model of osteoarthritis exhibited severe cartilage damage. The knockdown of AQP-1 decreased caspase-3 expression and activity in the cultured chondrocytes. In addition, the expression of AQP-1 positively correlated with caspase-3 expression and activity. Thus, the findings of our study, suggest that AQP-1 promotes caspase-3 activation and thereby contributes to chondrocyte apoptosis and to the development of osteoarthritis.

Osteoporosis and diabetes have become serious health problems worldwide. Previous studies have suggested that diabetes is associated with osteoporosis and increased fracture risk. However, the mechanism underlying diabetes‑induced osteoporosis remains to be elucidated. Therefore, the present study aimed to examine the mechanism underlying diabetes‑induced osteoporosis, and determine the protective effects of zinc, which is known to be closely associated with osteoporosis and diabetes. The results of the present study demonstrated that zinc inhibited advanced glycation end product (AGE)‑induced MC3T3‑E1 cell apoptosis by attenuating the production of reactive oxygen species, inhibiting caspase‑3 and caspase‑9 activation, and inhibiting the release of cytochrome c from between the mitochondria and the cytosol. Furthermore, zinc was found to protect cells against AGE‑induced apoptosis via the mitogen‑activated protein kinase/extracellular signal‑regulated kinase and phosphoinositide 3‑kinase/AKT signaling pathways. In conclusion, these findings enable a better understanding of the mechanism underlying diabetes‑induced osteoporosis, and may indicate a novel target for its prevention and treatment.